甲型H1N1流感肺炎影像学表现

目的 总结甲型H1N1流感肺炎影像学表现,提高对本病的认识。方法 回顾性分析17例确诊甲型H1N1流感肺炎患者胸部X线片及64层螺旋CT检查系列影像学资料。结果 17例甲型H1N1流感肺炎患者均有1次以上胸部计算机X线摄影术(CR)检查,其中8例接受CT检查。17例胸部X线及CT表现均以斑片或大片实变影合并磨玻璃密度影为主要表现。病变累及单侧肺野者4例,占23.53%;双侧肺野均受累者13例,占76.47%;随访病例均有不同程度的纤维化改变。结论 甲型H1N1流感肺炎X线及CT表现具有一定特征性。肺部病变以多叶段分布渗出性改变为其共有表现,病程后期两肺以纤维化表现为主。     

甲型H1N1流感的胸部影像学表现

目的 观察甲型H1N1流感患者的胸片及CT表现。 方法 回顾性分析51例甲型H1N1流感患者(实验室确诊47例,临床诊断4例)初始胸片及CT检查的病变表现形式、分布特点及病变程度。 结果 甲型H1N1流感患者的胸片及CT检查最主要表现是双侧或单侧多发磨玻璃密度影,伴或不伴单发或多发实变区。CT显示病变主要沿支气管血管周围中心肺区和(或)胸膜下区分布。 结论 影像学诊断甲型H1N1流感时,结合病史非常重要。     

支气管肺发育不良的CT表现

目的 观察支气管肺发育不良患儿胸部CT表现。方法 收集经临床确诊的支气管肺发育不良患儿42例,根据胎龄和吸入氧浓度分为轻、中、重度,均接受64层螺旋CT扫描及薄层重建,回顾性分析所有患儿的胸部CT表现。结果 胸部CT多表现为囊泡影(27/42,64.29%),双肺透光度减低、呈广泛或局部磨玻璃样改变(26/42,61.90%),条片状致密影(23/42,54.76%)及条索状、网格状、蜂窝状(16/42,38.10%);胸膜增厚4例,胸腔积液2例。囊泡影发生于双肺上下叶者15例(15/27,55.56%),其中10例发生于右肺中叶;仅发生于肺下叶者8例;仅发生于肺上叶者3例(3/27,11.11%);发生于双肺下叶及右肺中叶者1例。轻、中、重度支气管肺发育不良患儿中,囊泡影检出率分别为53.33%(8/15)、57.14%(8/14)、84.62%(11/13),差异无统计学意义(P=0.094);累及肺叶数(中位数)分别为1.0、1.5、4.0,差异有统计学意义(P<0.05)。结论 支气管肺发育不良常见的CT征象为囊泡影、局部或广泛磨玻璃影、致密影、条索状、网格状、蜂窝状影。囊泡影可发生于双肺,以肺下叶居多,胸膜下多见;囊泡影累及肺叶数越多,提示患儿临床表现越严重。     

重症型甲型H1N1流感9例胸部X线与CT特征分析

目的探讨重症型甲型H1N1流感的X线平片与CT特征。方法回顾性分析9例临床确诊的重症型甲型H1N1流感的X线与CT表现。结果首次X线胸部平片示双肺受累8例,单肺受累1例,8例行CT检查两肺均受累,1例死亡未行CT检查。受累肺叶3~5叶,受累肺段5~8个。9例均表现在两肺多叶,以中外带及下叶为甚,2例病变进展迅速,1例死亡。结论重症型甲型H1N1流感的主要影像学表现为：（1）病变主要发生在肺的外周;（2）两肺多叶受累,下肺野多于上肺野;（3）病变变化迅速;（4）两肺出现磨玻璃影、大片实变影,可见支气管气相,伴有胸膜增厚或少量胸水;（5）CT比胸片能更好地显示肺内病变特征。熟悉其影像学表现,密切结合临床和实验室检查可以做出明确诊断。     

甲型H1N1流感首次胸部CT表现初步分析

目的:探讨甲型H1N1流感首次胸部CT影像学特点.方法:回顾性分析临床确诊22例甲型H1N1流感患者的首次胸部CT表现.结果:22例患者中,男10例,女12例,年龄4～63岁,平均46岁.22例患者CT表现共有268个肺段病变,包括磨玻璃密度影218段、斑片状实变影30段、结节影20段.肺部病变分布在中外带17例,弥漫分布3例,内带2例.胸膜增厚15例,其中右侧12例、左侧10例、双侧7例.纵隔淋巴结肿大3例,胸腔积液2例.结论:甲型H1N1流感患者首次胸部CT表现特点为以双侧、多段、外带肺部磨玻璃密度影改变为主.     

重症甲型H1N1流感肺部的影像学表现

目的：探讨重症甲型H1N1流感患者的胸部X线和CT表现特征,以期提高对甲型H1N1流感的认识。方法：搜集我院2009年6月～2010年3月住院确诊重症甲型H1N1流感的患者11例,对其临床及影像学资料进行回顾性总结分析。结果：重症甲型H1N1流感临床的主要特征是持续高热、咳嗽,部分出现呼吸衰竭和神志改变。肺部影像学特点是：①早期最常见影像学表现为斑片状磨玻璃影;②发病后1～3天达到高峰,重症患者肺部病变变化较快且易反复;③治疗后患者肺部大部分病变可完全吸收,部分可见肺间质的改变。④肺部影像学表现与临床表现基本一致。结论：重症甲型H1N1流感患者的影像学表现可以反映病情变化,对指导临床治疗及判断预后具有重要的参考价值。     

胸部影像检查在甲型H1N1流感诊治中的应用及规范建议

目的探讨规范的胸部影像检查在甲型H1N1流感患者诊治中的应用价值.方法回顾性分析773例甲型H1N1流感患者的胸部X线、CT及高分辨率CT(HRCT)资料。结果 773例患者均接受胸部X线检查,78例接受CT检查,2例接受HRCT检查。胸部X线表现未见明显异常685例,占88.62%(685/773);双肺纹理增多、增粗、模糊等肺间质改变45例,占5.82%(45/773);肺间质改变伴肺门结构模糊28例,占3.62%(28/773);双肺间质改变合并多发斑片状渗出灶15例,占1.94%(15/773)。5例合并胸膜炎(5/773,0.65%)。结论甲型H1N1流感患者胸部影像学表现具有一定特征性,轻症患者X线检查多无明显异常,胸部X线及CT动态复查是了解病情进展的有效方法。     

甲型H1N1流感肺炎的胸部CT表现及动态变化特点

目的 探讨甲型H1N1流感肺炎的胸部CT表现及动态变化. 方法 对60例甲型H1N1流感确诊患者进行胸部CT扫描(含HRCT),回顾性分析、比较病变的影像学特点及动态变化并进行半定量CT评分. 结果 甲型H1N1流感胸部CT表现及动态变化特点:①主要表现为片状肺实质渗出病灶,早期和吸收期主要CT表现为磨玻璃密度影;②两肺小叶性或节段性散在分布,以胸膜下和支气管周围多见,下叶较重;③肺组织、胸膜及纵隔受累可同时存在;④病程早期CT评分4.41且逐渐下降,渗出性病灶短期内吸收较快,后期遗留纤维化病变CT评分1.64分. 结论甲型H1N1流感肺炎的动态胸部CT表现具有一定特征性.熟悉其胸部CT表现有助于该病的诊断、鉴别诊断与疗效观察,但确诊需依靠流行病学史及实验室检查.     

新型冠状病毒肺炎CT表现及动态变化

目的 [JP2]观察新型冠状病毒肺炎（COVID-19）CT表现及其动态变化。方法 回顾性分析45例经病毒核酸检测确诊、且具有完整动态胸部HRCT资料的COVID-19患者，复查间隔时间48~72 h。结果 29例于发病3天内接受CT检查，21例（21/29，72.41%）胸部见磨玻璃密度影，8例（8/29，27.59%）见磨玻璃密度影伴局部实变，其中2例（25.00%，2/8）为单发结节；26例（26/29，89.66%）病灶呈不规则形或扇形，3例呈类圆形（3/29，10.34%）。16例于发病3天以上接受CT检查，病灶进展。首次复查CT病变均有变化，其中14例（14/45，31.11%）呈单纯磨玻璃密度影，27例（27/45，60.00%）以磨玻璃样密度影为主且有肺实变，4例（4/45，8.89%）以肺实变为主。38例于发病7~10天接受第2次复查，25例（25/38，65.79%）病变范围缩小，4例病灶范围增大（4/38，10.53%），1例（1/38，2.63%）病灶范围同前；8例（8/38，21.05%）原有病灶密度减低但出现新发病灶。其余7例因病变进展而未能接受复查。结论 胸部HRCT能清晰显示COVID-19疾病过程中的影像学变化，有助于指导临床早诊断、早隔离、早治疗，并可作为评价COVID-19临床综合治疗效果的依据。     

CT联合胸部X线检查对诊断早期肺部感染准确率的影响

目的分析CT联合胸部X线检查肺部感染早期诊断准确率的影响。方法选取我院2015年8月~2017年10月收诊疑似肺部感染患者123例,均行胸部X线、CT检查及痰液培养。以痰液培养为金标准,对比胸部X线联合CT与单一胸部X线的准确率。123例疑似肺部感染患者中,痰液培养结果显示阳性92例、阴性31例。胸部X线+CT诊断准确率为86.96%(80/92),较单一胸部X线61.96%(57/92)高,差异具有统计学意义(P0.05);80例胸部X线+CT确诊患者中,CT影像学显示非特异性细菌感染34例、病毒感染4例、真菌感染19例、混合感染23例;非特异性细菌感染中实变影占67.65%(23/34)、磨玻璃影占14.71%(5/34)、结节影占11.76%(4/34)、线样影或磨玻璃影占5.88%(2/34);病毒感染中实变影占0.00%(0/4)、磨玻璃影占75.00%(3/4)、结节影占0.00%(0/4)、线样影或磨玻璃影占25.00%(1/4);真菌感染中实变影占21.05%(4/19)、磨玻璃影占47.37%(9/19)、结节影占26.32%(5/19)、线样影或磨玻璃影占5.26%(1/19);混合感染中实变影占21.74%(5/23)、磨玻璃影占65.22%(15/23)、结节影占8.70%(2/23)、线样影或磨玻璃影占4.35%(1/23)。结论 CT联合胸部X线检查可提高肺部感染早期诊断准确率。     

色素失禁症11例临床特征分析

【目的】探讨色素失禁症患儿临床特征,提高对该病的认识。【方法】对本院2004年1月至2013年12月收治的色素失禁症11例患儿临床特点进行分析。【结果】11例患儿中10例为女性,1例男性,2例为双胞胎早产儿。11例均有皮肤受累,神经系统受累发生惊厥2例,眼部受累2例。6例外周血嗜酸性粒细胞数比例明显升高,4例行皮肤活检,病理结果疱内有大量嗜酸性细胞支持诊断,1例核转录因子κB必需调节器（NEMO）基因缺失。【结论】色素失禁症是一种少见的 X连锁的显性遗传病,新生儿期皮肤损害显著,可累及多系统,眼部及神经系统病变严重,应得到早期诊断;皮肤病理和染色体的基因分析是确诊方法,应对患儿进行定期随访。     

The sphingosine-1-phosphate (S1P) lysophospholipid receptor S1P3 regulates MAdCAM-1+ endothelial cells in splenic marginal sinus organization

Marginal zones (MZs) are microdomains in the spleen that contain various types of immune cells, including MZ B cells, MOMA1(+) metallophilic macrophages, and mucosal addressin cell adhesion molecule 1 (MAdCAM-1)(+) endothelial cells. MAdCAM-1(+) and MOMA1(+) cells line the sinus, that separates MZs from splenic follicles. Here we show that a receptor for the lysophospholipid sphingosine-1-phosphate (S1P), S1P(3), is required for normal numbers of splenic immature and MZ B cells, and for S1P-induced chemotaxis of MZ B cells. S1P(3) is also essential for proper alignment of MOMA1(+) macrophages and MAdCAM-1(+) endothelial cells along the marginal sinus. The lack of cohesion of the marginal sinus in S1P(3)(-/-) mice affects MZ B cell functions, as wild-type (WT) MZ B cells migrate more into S1P(3)(-/-) follicles than into WT follicles after treatment with lipopolysaccharide. Additionally, short-term homing experiments demonstrate that WT MZ B cells home to the S1P(3)(-/-) spleen in increased numbers, suggesting a role for the marginal sinus in regulating MZ B cells numbers. Moreover, S1P(3)(-/-) mice are defective in mounting immune responses to thymus-independent antigen type 2 due to defects in radiation-resistant cells in the spleen. These data identify lysophospholipids and the S1P(3) receptor as essential regulators of the MZ sinus and its role as a barrier to the follicle.     

Suppression of WNK1-SPAK/OSR1 Attenuates Bone Cancer Pain by Regulating NKCC1 and KCC2

Our preliminary experiment indicated the activation of with-nolysine kinases 1 (WNK1) in bone cancer pain (BCP) rats. This study aimed to investigate the underlying mechanisms via which WNK1 contributed to BCP. A rat model of BCP was induced by Walker-256 tumor cell implantation. WNK1 expression and distribution in the lumbar spinal cord dorsal horn and dorsal root ganglion were examined. SPS1-related proline/alanine-rich kinase (SPAK), oxidative stress-responsive kinase 1 (OSR1), sodium-potassium-chloride cotransporter 1 (NKCC1), and potassium-chloride cotransporter 2 (KCC2) expression were assessed. Pain behaviors including mechanical allodynia and movement-evoked pain were measured. BCP rats exhibited significant mechanical allodynia, with increased WNK1 expression in the dorsal horn and dorsal root ganglion neurons, elevated SPAK/OSR1 and NKCC1 expression in the dorsal root ganglion, and decreased KCC2 expression in the dorsal horn. WNK1 knock-down by small interfering alleviated mechanical allodynia and movement-evoked pain, inhibited WNK1-SPAK/OSR1-NKCC1 activities, and restored KCC2 expression. In addition, closantel (a WNK1-SPAK/OSR1 inhibitor) improved pain behaviors, downregulated SPAK/OSR1 and NKCC1 expression, and upregulated KCC2 expression in BCP rats. Activation of WNK1-SPAK/OSR1 signaling contributed to BCP in rats by modulating NKCC1 and KCC2 expression. Therefore, suppression of WNK1-SPAK/OSR1 may serve as a potential target for BCP therapy.PerspectiveOur findings demonstrated that the WNK1-SPAK/OSR1 signaling contributed to BCP in rats via regulating NKCC1 and KCC2. Suppressing this pathway reduced pain behaviors. Based on these findings, the WNK1-SPAK/OSR1 signaling may be a potential target for BCP therapy.     

长链非编码RNA DBH-AS1通过下调AKT1表达抑制胰腺癌进展

目的与背景 本研究旨在检测长链非编码RNA DBH-AS1在胰腺癌中的表达情况,探讨DBH-AS1在胰腺癌进展中的潜在分子作用。方法 采用实时定量PCR检测基因表达。细胞增殖、成克隆生长和迁移侵袭能力分别通过CCK-8、克隆形成和transwell检测。蛋白质水平用免疫印迹法测定。结果GEPIA数据库和定量PCR结果证实,DBH-AS1在胰腺癌组织中表达下调,与癌旁正常胰腺组织相比差异均有统计学意义(P 均＜0.05)。在胰腺癌肿瘤组织中DBH-AS1的低表达与肿瘤分化差、TNM分期晚期、淋巴结转移、以及预后不良(无瘤生存时间和总体生存时间)有关(P均＜0.05)。DBH-AS1基因敲除可促进胰腺癌细胞的增殖、克隆形成、迁移和侵袭能力,与对照组相比差异均有统计学意义(P均＜0.05)。机制研究表明,在胰腺癌中DBH-AS1通过下调AKT1表达抑制mTOR信号通路。结论DBH-AS1通过降低AKT1的表达抑制胰腺癌的进展。     

超声造影在钝性腹部创伤患者诊断中的应用价值

Purpose: Trauma is the main leading cause of disability and death in young adult population, of which blunt abdominal trauma is one of the most common types of injury, rapid identification of organ injury in blunt abdominal trauma patients is crucial. The purpose of this study was to evaluate the diagnostic ability of contrast-enhanced ultrasound (CEUS) in adults with blunt abdominal trauma. Methods: Patients with blunt abdominal trauma attending the emergency department of the Second Hospital of Chongqing Medical University from 2020.10 to 2023.2 were included in this study, general demographic and injuries procedure were collected, organ injuries were assessed by comparing the results of enhanced computed tomography (CECT) and CEUS with American Association for Trauma Surgery standards. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of CEUS were calculated by drawing cross-tabulations using CECT as a standard.The diagnostic performance between CEUS and CECT were compared by McNemar-Bowke test. The diagnostic consistency between CEUS and CECT was analyzed by kappa consistency test, the cost differences were compared by rank sum test, and the adverse reactions of CEUS were reported. Results: A total of 42 patients with blunt abdominal trauma were included, predominantly male patients. 30 injury patients were found by CECT and 29 injury patients were found by CEUS, and the sensitivity of CEUS was found to be 93.33%, specificity 91.67%, positive predictive value 96.55%, negative predictive value 84.62%, and diagnostic accuracy 92.86%, respectively. McNemar-Bowke test showed that there was no statistical difference in diagnostic performance between CEUS and CECT (χ2=1,P=0.317). Kappa consistency test found that its Kappa value was 0.966. No adverse events were observed and the single time cost was significantly lower than that of CECT (￥806 vs. ￥1657,P=0.000). Conclusion: CEUS is a safe, effective, convenient, low-cost, and radiation-free imaging method that can be used as an effective alternative method to CECT in blunt abdominal trauma patients.     

Transendothelial Migration of Megakaryocytes in Response to Stromal Cell-derived Factor 1 (SDF-1) Enhances Platelet Formation

Although thrombopoietin has been shown to promote megakaryocyte (MK) proliferation and maturation, the exact mechanism and site of platelet formation are not well defined. Studies have shown that MKs may transmigrate through bone marrow endothelial cells (BMEC), and release platelets within the sinusoidal space or lung capillaries. In search for chemotactic factor(s) that may mediate transmigration of MKs, we have discovered that mature polyploid MKs express the G protein–coupled chemokine receptor CXCR4 (Fusin, LESTR). Therefore, we explored the possibility that stromal cell–derived factor 1 (SDF-1), the ligand for CXCR4, may also induce transendothelial migration of mature MKs. SDF-1, but not other CXC or CC chemokines, was able to mediate MK migration (ED₅₀ = 125 pmol/liter). The MK chemotaxis induced by SDF-1 was inhibited by the CXCR4-specific mAb (12G5) and by pertussis toxin, demonstrating that signaling via the G protein–coupled receptor CXCR4 was necessary for migration. SDF-1 also induced MKs to migrate through confluent monolayers of BMEC by increasing the affinity of MKs for BMEC. Activation of BMEC with interleukin 1β resulted in a threefold increase in the migration of MKs in response to SDF-1. Neutralizing mAb to the endothelial-specific adhesion molecule E-selectin blocked the migration of MKs by 50%, suggesting that cellular interaction of MKs with BMEC is critical for the migration of MKs. Light microscopy and ploidy determination of transmigrated MKs demonstrated predominance of polyploid MKs. Virtually all platelets generated in the lower chamber also expressed CXCR4. Platelets formed in the lower chamber were functional and expressed P-selectin (CD62P) in response to thrombin stimulation. Electron microscopy of the cells that transmigrated through the BMEC monolayers in response to SDF-1 demonstrated the presence of intact polyploid MKs as well as MKs in the process of platelet formation. These results suggest that SDF-1 is a potent chemotactic factor for mature MKs. Expression of CXCR4 may be the critical cellular signal for transmigration of MKs and platelet formation.     

Identification of C-C Chemokine Receptor 1 (CCR1) as the Monocyte Hemofiltrate C-C Chemokine (HCC)-1 Receptor

Hemofiltrate C-C chemokine (HCC)-1 is a recently cloned C-C chemokine that is structurally similar to macrophage inflammatory protein (MIP)-1α. Unlike most chemokines, it is constitutively secreted by tissues and is present at high concentrations in normal human plasma. Also atypical for chemokines, HCC-1 is reported not to be chemotactic for leukocytes. In this paper, we have investigated the chemokine receptor usage and downstream signaling pathways of HCC-1. Cross-desensitization experiments using THP-1 cells suggested that HCC-1 and MIP-1α activated the same receptor. Experiments using a panel of cloned chemokine receptors revealed that HCC-1 specifically activated C-C chemokine receptor (CCR)1, but not closely related receptors, including CCR5. HCC-1 competed with MIP-1α for binding to CCR1-transfected cells, but with a markedly reduced affinity (IC₅₀ = 93 nM versus 1.3 nM for MIP-1α). Similarly, HCC-1 was less potent than MIP-1α in inducing inhibition of adenylyl cyclase in CCR1-transfected cells. HCC-1 induced chemotaxis of freshly isolated human monocytes, THP-1 cells, and CCR1-transfected cells, and the optimal concentration for cell migration (100 nM) was ∼100-fold lower than that of MIP-1α (1 nM). These data demonstrate that HCC-1 is a chemoattractant and identify CCR1 as a functional HCC-1 receptor on human monocytes.     

myc拮抗基因Mad1、Mxi1和Rox在白血病细胞中的表达和突变

目的分析Madl、Mxil和Rox基因突变在白血病发病中的作用。方法利用逆转录．聚合酶链反应（1iT-PCR）、单链构象多态性（SSCP）分析及DNA序列分析技术检测了26例初治急性白血病（AL）患者、30名健康对照者和7种白血病细胞株中Madl、Mxil和Rox基因表达及突变情况。结果liT-PCR检测结果显示所有标本中均可检测到Madl、Mxil和Rox基因的表达；SSCP分析结果显示所有标本中有4个位点发生多态性改变：Madl中2个位点，Mxil和Rox中各1个位点。DNA序列分析显示所有标本中有9个位点发生错义突变：Madl中2个位点均发现于初治AL患者；Mxil中4个位点，其中3个位点发现于初治AL患者，1个位点发现于KGl细胞株；Rox中3个位点均发现于初治AL患者。26例初治AL患者Madl、Mxil和Rox基因的突变发生分别为2例、3例和3例。结论首次在AL患者细胞中发现Madl、Mxil和Rox基因突变，提示Madl、Mxil和Rox基因的突变可能与白血病的发病有关。